Acon

There are 3 papers on Acon in aging research: none in people yet, 3 in animals.

Gene

3 papers study it4 findings

NCBI GeneTaxon

See all 3 papers on Acon

At a glance

The findings reach worms or flies, none yet in people. 1 lab in 1 country.

None of its findings points the other way.

Worms or flies: a single group. Cells, mice and humans: nothing yet.
  • 1 lab in 1 country
  • Funder: National Research Foundation of Korea
  • Model organisms3

Effects

4

Mitophagy

upin flies1

1 study
  1. Acon increases mitophagy in flies (labeled with mt-Keima).

    “mAcon1 overexpression in Kenyon cells induced mitophagy labeled with mt-Keima and improved learning ability.”

    Model organismslabeled with mt-KeimaKenyon cell

    Mitochondrial aconitase 1 regulates age-related memory impairment via autophagy/mitophagy-mediated neural plasticity in middle-aged flies

    Aging cell

More on Mitophagy

Autophagy

upin flies1

1 study
  1. Acon increases autophagy in flies (measured by Atg8a-II and p62 levels).

    “Autophagy activity and efficacy determined by the positive and negative changes in the expression levels of Atg8a-II and p62 were proportional to the expression level of mAcon1.”

    Model organismsmeasured by Atg8a-II and p62 levels

    Mitochondrial aconitase 1 regulates age-related memory impairment via autophagy/mitophagy-mediated neural plasticity in middle-aged flies

    Aging cell

More on Autophagy

Learning and memory

upin flies1

1 study
  1. Acon improves learning and memory in flies (age-related memory impairment, shown by neuronal overexpression).

    “Neuronal overexpression of mAcon1 extended its lifespan and improved AMI.”

    Model organismsage-related memory impairment, shown by neuronal overexpressionneuron

    Mitochondrial aconitase 1 regulates age-related memory impairment via autophagy/mitophagy-mediated neural plasticity in middle-aged flies

    Aging cell

Lifespan

upin flies1

1 study
  1. Acon extends lifespan in flies (shown by neuronal overexpression).

    “Neuronal overexpression of mAcon1 extended its lifespan and improved AMI.”

    Model organismsshown by neuronal overexpressionneuron

    Mitochondrial aconitase 1 regulates age-related memory impairment via autophagy/mitophagy-mediated neural plasticity in middle-aged flies

    Aging cell

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